The invention generally relates to power control, and more particularly, to controlling the energy delivered to a patient for more effective energy transfer.
The heart beat in a healthy human is controlled by the sinoatrial node ("S-A node") located in the wall of the right atrium. The S-A node generates electrical signal potentials that are transmitted through pathways of conductive heart tissue in the atrium to the atrioventricular node ("A-V node") which in turn transmits the electrical signals throughout the ventricle by means of the His and Purkinje conductive tissues. Improper growth of or damage to the conductive tissue in the heart can interfere with the passage of regular electrical signals from the S-A and A-V nodes. Electrical signal irregularities resulting from such interference can disturb the normal rhythm of the heart and cause an abnormal rhythmic condition referred to as cardiac arrhythmia.
Electrophysiological ablation is a procedure often successful in terminating cardiac arrhythmia. This procedure involves applying sufficient energy to the interfering tissue to ablate that tissue thus removing the irregular signal pathway. However, before the ablation procedure can be carried out, the interfering tissue must first be located.
One location technique involves an electrophysiological mapping procedure whereby the electrical signals emanating from the conductive endocardial tissues are systematically monitored and a map is created of those signals. By analyzing that map, the interfering electrical pathway can be identified. A conventional method for mapping the electrical signals from conductive heart tissue is to percutaneously introduce an electrophysiology ("EP") catheter having mapping electrodes mounted on its distal extremity. The catheter is maneuvered to place those electrodes in contact with or in close proximity to the endocardium of the patient's heart. By monitoring the electrical signals at the endocardium, aberrant conductive tissue sites responsible for the arrhythmia can be pinpointed.
Once the origination point for the arrhythmia has been located in the tissue, the physician may use an ablation procedure to destroy the tissue causing the arrhythmia in an attempt to remove the electrical signal irregularities and restore normal heart beat or at least an improved heart beat. Successful ablation of the conductive tissue at the arrhythmia initiation site usually terminates the arrhythmia or at least moderates the heart rhythm to acceptable levels.
The distal end of an EP catheter may include mapping electrodes as well as an ablation device for performing the ablation procedure. One type of ablation device includes an ablation electrode that emits radio frequency ("RF") energy to heat the target tissue to a temperature high enough to cause ablation of that tissue. Another type of ablation devices comprises an ultrasonic device, such as a piezoelectric device.
As the ablation procedure progresses, heat is generated and the surrounding blood is exposed to this heat. At approximately 100.degree. C., charring and boiling of the blood take place. Coagulation may also occur. Charring is particularly troublesome at the surface of the ablation device because emboli may form on the surface of the device to an extent that the catheter must be removed and cleaned before the procedure can continue. Furthermore, charring and coagulation can cause a substantial increase in the impedance and a corresponding decrease in the power delivery to the tissue. Too great a rise in impedance can result in sparking and thrombus formation within the heart, both of which are undesirable.
Because part of the ablation transducer is in contact with the blood in the heart, blood boiling, emboli development, and clotting can result if the surface temperature of the transducer exceeds 90-100.degree. C. If this occurs, the ablation procedure must be stopped regardless of whether the entire ablation procedure has been completed. The catheter must then be removed from the patient, the attached necrotic tissue removed, and the catheter reinserted into the patient. Such cleaning processes require extra time and unduly prolong the ablation procedure. To avoid such undesirable circumstances, a temperature sensor may be incorporated at the distal end of the catheter to monitor and maintain a selected temperature during ablation. The ablation process can then be controlled so that the temperature is not allowed to increase above a predetermined level.
In many cases, the target tissue extends relatively deeply in the endocardium. To successfully ablate that tissue, deeper lesions are necessary. However, merely increasing the power applied to the ablation device does not necessarily result in a lesion of greater depth. Power at too high a level can damage the delivery instrument, or cause charring and boiling of the surrounding blood and tissues, thereby necessitating termination of the application of energy and prematurely shortening the ablation procedure before the lesion can be developed to the desired depth.
Hence, those skilled in the art have recognized the need to improve the delivery of energy to the patient. Improved delivery of ablation energy is needed to produce deeper lesions in the heart tissue while at the same time, controlling the temperature developed at the site. The present invention fulfills these needs and others.